PMID- 14726223
OWN - NLM
STAT- MEDLINE
DCOM- 20040928
LR  - 20190922
IS  - 1043-6618 (Print)
IS  - 1043-6618 (Linking)
VI  - 49
IP  - 3
DP  - 2004 Mar
TI  - Inhibitory effect of polypeptide from Chlamys farreri on ultraviolet A-induced 
      oxidative damage on human skin fibroblasts in vitro.
PG  - 265-74
AB  - We have previously reported that polypeptide from Chlamys farreri (PCF) inhibits 
      the oxidative damage of ultraviolet A (UVA) on HeLa cells in vitro [Acta Pharm. 
      Sin. 23 (2002) 961]. To further elucidate a possible role for PCF on UVA-damaged 
      normal human cells, we established the oxidative damage models of normal human 
      dermal fibroblasts (NHDF) exposed to UVA to study the protective effect of PCF on 
      human dermal fibroblasts in vitro. In this study, 
      3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) method was 
      used to detect the cell viability. The intracellular superoxide dismutase (SOD), 
      glutathione peroxidase (GSH-px), catalase (CAT), xanthine oxidase (XOD), 
      malondialdehyde (MDA), reactive oxygen species (ROS), total antioxidative 
      capacity (T-AOC), and anti-superoxide anion capacity (A-ASC) were measured. The 
      effect of PCF on UVA-induced apoptosis were investigated by Annexin V-FITC assay. 
      Intracellular calcium was determined with the calcium-sensitive fluorochrome 
      Fluo-3, and mitochondrial transmembrane potential with rhodamine 123. Comet assay 
      was employed to detect the UVA-induced DNA damage. The ultrastructure of cell was 
      observed under transmission electron microscope. The results indicated that PCF 
      could greatly enhance the viability of NHDF and markedly promote SOD, GSH-px, 
      T-AOC, and A-ASC, while the amounts of MDA and ROS, the activity of XOD were 
      decreased. PCF could inhibit UVA-induced apoptosis and DNA damage in NHDF. The 
      concentration of cellular free calcium was decreased and the mitochondrial 
      transmembrane potential was increased by PCF. In ultrastructure of NHDF, PCF 
      could greatly decrease UVA-induced damage, especially membrane. Our results 
      suggest that the supplementation of PCF appears to reduce the UVA-induced normal 
      human dermal fibroblasts damage efficiently. It may be involved in the PCF's 
      abilities of scavenging oxygen free radical, inhibiting lipid peroxidation, 
      increasing antioxidative enzymes, decreasing intracellular calcium and protection 
      of membrane structure in NHDF irradiated by UVA.
FAU - Han, Yan-Tao
AU  - Han YT
AD  - Medical College, Qingdao University, Qingdao, Shandong, 266021, China.
FAU - Han, Zhi-Wu
AU  - Han ZW
FAU - Yu, Guo-Ying
AU  - Yu GY
FAU - Wang, Yue-Jun
AU  - Wang YJ
FAU - Cui, Rui-Yao
AU  - Cui RY
FAU - Wang, Chun-Bo
AU  - Wang CB
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Pharmacol Res
JT  - Pharmacological research
JID - 8907422
RN  - 0 (Peptides)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/physiology
MH  - Cell Survival/drug effects/physiology/radiation effects
MH  - Cells, Cultured
MH  - Fibroblasts/drug effects/physiology/*radiation effects
MH  - Humans
MH  - Male
MH  - Mollusca
MH  - Oxidative Stress/physiology/*radiation effects
MH  - Peptides/*pharmacology
MH  - Shellfish
MH  - Skin/drug effects/*radiation effects
MH  - Ultraviolet Rays/*adverse effects
EDAT- 2004/01/17 05:00
MHDA- 2004/09/29 05:00
CRDT- 2004/01/17 05:00
PHST- 2004/01/17 05:00 [pubmed]
PHST- 2004/09/29 05:00 [medline]
PHST- 2004/01/17 05:00 [entrez]
AID - S1043661803003098 [pii]
AID - 10.1016/j.phrs.2003.09.009 [doi]
PST - ppublish
SO  - Pharmacol Res. 2004 Mar;49(3):265-74. doi: 10.1016/j.phrs.2003.09.009.